A 64-year-old retired teacher, Ms M, presented with a 3-4 week history of generalized malaise, nausea and poor appetite following a flu-like illness in last August. She denied difficulty with urination or burning during urination. She also denied symptoms of fever, chills, cough or phlegm. She stated she had no history of abnormal bowel movements, vomiting, bleeding per rectum or melena, and no cardiac history of angina or heart failure. She’d never had ankle swelling, orthopnea or paroxysmal nocturnal dyspnea, nor any documented cancer or sarcoidosis.
She has a history, however, of diabetes mellitus for 25 years (following pancreatic surgery for a benign tumour), hypertension and carotid artery disease. Ms M underwent carotid endarterectomy in 2007 and suffered a right hemispheric stroke in 2009. She’s been wheel-chair dependent since. She also had a previous thyroidectomy for a benign tumour about 10 years ago, and has a history of mild diabetic retinopathy that hasn’t required laser therapy yet. There was no documented history of proteinuria or diabetic nephropathy.
Her medications include: insulin, aspirin, levothyroxine, paroxetine and temazepam. She smoked 1-pack per day for 40 years and quit in 2009, following her stroke.
The physical examination was remarkable for a woman of Ms M’s age and thin build, with a blood pressure of 134/70 mm Hg and regular rhythm. There was no evidence of orthostatic changes. Her neck examination was remarkable for thyroidectomy and a right carotid endarterectomy scar with bilateral carotid bruits. Jugular venous pressure was not elevated. No masses or lymph nodes were noted in her neck. Her heart sounds were normal and there were no murmurs. Ms M’s lungs were clear with fair air entry bilaterally. Her abdomen was soft with an irregular right paramedian scar without any masses. There was no peripheral edema. The neurological exam revealed an alert woman with residual left-sided weakness.
Investigations in the emergency department show: hemoglobin of 136 gm/L, glucose of 16.7 mmol/L, normal electrolytes with serum potassium of 4.2 mmol/L, elevated BUN of 43.3 mmol/L, serum creatinine of 444 µmol/L. Urinalysis shows traces of protein with inactive urinary sediment. She had a serum creatinine of 99 µmol/L in 2009.
Further investigations performed show normal renal ultrasound (no obstruction, normal renal size and echogenicity), slightly low serum albumin of 34 gm/L, elevated serum calcium of 3.63 mmol/L (2.02-2.6 mmol/L), slightly high serum phosphorus of 1.98 mmol/L (0.87-1.45 mmol/L), normal CK of 41, a faint IgG Kappa band on serum immunoelectrophoresis.
What’s your diagnosis? What is your management plan?
Ms M was noted to have marked hypercalcemia with a serum calcium of 3.63. She was admitted to the hospital and started on intravenous saline and furosemide (Lasix) to control her hypercalcemia. With the lowering of her serum calcium, her serum creatinine improved and decreased to 161 µmol/L from 444 µmol/L. Further investigations were requested and the patient was discharged home. But about a week later she presented again with nausea and vomiting, and again her serum calcium was elevated at 3.03 mmol/L with serum creatinine of 323 µmol/L.
Patients with chronic renal failure can have hypercalcemia from tertiary hyperparathyroidism but not to this extent. This occurs with a longstanding history of renal failure — not the case in Ms M.
Possibilities of primary hyperparathyroidism, sarcoidosis and underlying malignancy, including the possibility of multiple myeloma, were entertained. A bone marrow examination was negative for plasma cell disorder (like multiple myeloma). Parathyroid hormone level and 24-hour urine calcium was requested.
Ms M’s parathyroid level was elevated at 124 (normal 1-8) and a 24-hour urine calcium was elevated at 8.2 mmol/day (normal < 7.5 mmol/day). A parathyroid sestamibi scan raised the possibility of parathyroid adenoma, although it was difficult to interpret because of a previous thyroidectomy.
The patient was referred for surgery and a 5x4 cm right parathyroid adenoma was removed. Following that her serum calcium levels returned to lower than normal (hungry bones phenomenon).
This is an interesting case of renal failure secondary to hypercalcemic nephropathy secondary to a large parathyroid adenoma. In view of Ms M’s history of a previous pancreatic tumour surgery 25 years ago and thyroidectomy about 10-years ago, we feel that this was a complex case of MEN (multiple endocrine neoplasia), type 1 syndrome.
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